General Information of the m6A Target Gene (ID: M6ATAR00634)
Target Name Neuroblast differentiation-associated protein AHNAK (AHNAK)
Synonyms
Desmoyokin
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Gene Name AHNAK
Chromosomal Location 11q12.3
Function
May be required for neuronal cell differentiation.
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Gene ID 79026
Uniprot ID
AHNK_HUMAN
HGNC ID
HGNC:347
Ensembl Gene ID
ENSG00000124942
KEGG ID
hsa:79026
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
AHNAK can be regulated by the following regulator(s), and cause disease/drug response(s). You can browse detail information of regulator(s) or disease/drug response(s).
Browse Regulator
Browse Disease
Methyltransferase-like 3 (METTL3) [WRITER]
Representative RNA-seq result indicating the expression of this target gene regulated by METTL3
Cell Line MOLM-13 cell line Homo sapiens
Treatment: shMETTL3 MOLM13 cells
Control: MOLM13 cells
GSE98623
Regulation
logFC: 1.10E+00
p-value: 5.50E-75
More Results Click to View More RNA-seq Results
Representative RIP-seq result supporting the interaction between AHNAK and the regulator
Cell Line MDA-MB-231 Homo sapiens
Regulation logFC: 1.20E+00 GSE60213
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary METTL3 knockout in the limbal stem cells promotes the in vivo cell proliferation and migration, leading to the fast repair of corneal injury. In addition, m6A modification profiling identified stem cell regulatory factors Neuroblast differentiation-associated protein AHNAK (AHNAK) and DDIT4 as m6A targets.
Target Regulation Up regulation
Responsed Disease Corneal injury ICD-11: NA06.4
Cell Process Cell proliferation
Cell migration
In-vitro Model CGC (Conjunctival goblet cells)
In-vivo Model Mettl3fl/wt mice were generated as previously described. Mettl3fl/wt mice were crossed with K14CreER mice to obtain K14creER/Mettl3fl/fl (cKO) mice. Mettl3 cKO and control mice were injected with tamoxifen and then were subjected to corneal alkali burn treatment. The right eye was the experimental eye, and the left eye was the control eye. The mice were sacrificed at 24 hours, 7 days, 14 days, 35 days, and 56 days after injury. Six mice were taken from each period. Both eyes were removed, frozen in OCT (n = 4), fixed in 4% paraformaldehyde, and embedded in conventional paraffin (n = 2).
Corneal injury [ICD-11: NA06]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary METTL3 knockout in the limbal stem cells promotes the in vivo cell proliferation and migration, leading to the fast repair of corneal injury. In addition, m6A modification profiling identified stem cell regulatory factors Neuroblast differentiation-associated protein AHNAK (AHNAK) and DDIT4 as m6A targets.
Responsed Disease Corneal injury [ICD-11: NA06.4]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
Target Regulation Up regulation
Cell Process Cell proliferation
Cell migration
In-vitro Model CGC (Conjunctival goblet cells)
In-vivo Model Mettl3fl/wt mice were generated as previously described. Mettl3fl/wt mice were crossed with K14CreER mice to obtain K14creER/Mettl3fl/fl (cKO) mice. Mettl3 cKO and control mice were injected with tamoxifen and then were subjected to corneal alkali burn treatment. The right eye was the experimental eye, and the left eye was the control eye. The mice were sacrificed at 24 hours, 7 days, 14 days, 35 days, and 56 days after injury. Six mice were taken from each period. Both eyes were removed, frozen in OCT (n = 4), fixed in 4% paraformaldehyde, and embedded in conventional paraffin (n = 2).
References
Ref 1 METTL3-Mediated m(6)A RNA Modification Regulates Corneal Injury Repair. Stem Cells Int. 2021 Oct 22;2021:5512153. doi: 10.1155/2021/5512153. eCollection 2021.